Glaucomatous Optic Nerve Damage

Glaucomatous Optic Nerve Damage

May 17, 2022

The optic nerve is composed of approximately 1.5 million nerve fibers at the back of the eye that carry visual messages from the retina to the brain.

When light hits the retina, the photoreceptors (light-sensitive cells) receive and transmit this information to other specialized cells, including the final cell type in the chain, called the retinal ganglion cells.

These cells reside in the retina, but their output “cables” or “fibers,” called axons, extend from the head of the optic nerve at the back of the eye to the brain. Therefore, the retinal ganglion cell plays a critical role as the output nerve cell of the eye that transmits visual information to the brain.

When the eyes are examined, the optic nerve is actually visualized by the eye doctor with the help of special lenses. The axons of the optic nerve are bundled and insert in the back of the eye, and this “optic disc” is seen in the back of the eye along with blood vessels.

In optic nerve degeneration related to glaucoma, the optic disc displays changes that are characteristic of glaucoma, which your doctor may refer to as “cupping.”

When considering glaucoma, focus historically has been on intraocular pressure (IOP). But other types of pressures are involved and should be on optometrists’ radar, according to Mark T. Dunbar, OD, FAAO, director of optometric services, Bascom Palmer Eye Institute, University of Miami Health System, Key Largo, Florida.

Dunbar explained that while the general principles for managing patients with glaucoma seem straightforward—the higher the IOP, the greater the risks are of both glaucomatous damage and disease progression—other factors contribute to optic nerve damage and determine an individual’s susceptibility to damage from IOP.

The current confounding factor is that there are no other effective treatments for glaucoma; lowering the IOP is the only avenue available.

Factors contributing to glaucoma - Many patient scenarios are not straightforward. For example, Dunbar posed, some patients with high IOPs do not have glaucoma and have normal optic nerves with ocular hypertension.

The reverse is also true: A patient can have IOP in the normal range and severe glaucoma. Other things that can show up in an examination are suspicious optic nerves seen on imaging or borderline high IOPs that leave the clinicians in a state of uncertainly about whether or not to begin treatment, he explained.

He described a representative case of an 80-year-old woman with IOPs of approximately 12 mm Hg and disc hemorrhages whose glaucoma was progressing.

Things to watch Blood pressure - Investigators suggested 3 decades ago that systemic hypotension and decreases in nocturnal blood pressure were instrumental in glaucoma progression. A combination of lowest blood pressure levels and the highest IOP levels at night are risk factors for disease progression.

“The combination of the 2 may result in a critical ocular perfusion pressure (OPP) in susceptible people, those with faulty autoregulation,” Dunbar said.

Ocular perfusion pressure - OPP is defined as the relative pressure at which blood enters the eye, or the ocular arterial pressure minus the IOP.

“OPP is a delicate balance between the [IOP] and blood pressure. Low OPP is a risk factor for progression resulting from low blood pressure and/or high IOP,” he said. The relationship between OPP and glaucoma, however, has not been confirmed.

Dunbar explained that because OPP is difficult to measure, there is no widely accepted standardized method to evaluate blood flow and interpret the results. Currently, blood flow measurements are not used to diagnose or manage glaucoma.

Cerebrospinal fluid pressure - Two retrospective studies conducted by John Berdahl, MD, in 2008, included close to 100,000 patients who underwent a lumbar puncture. Of those who underwent an ocular examination, 217 had primary open-angle glaucoma (POAG).

In the first study, authors concluded that intracranial pressure was significantly lower in patients with POAG compared with controls without glaucoma.

In the second study, authors also concluded that the intracranial pressure was significantly lower in patients with POAG and normal-tension glaucoma, while the intracranial pressure was significantly higher in those with ocular hypertension. “In the normal state, IOP and cerebrospinal fluid have minimal translaminar pressure difference.

When the difference between the two is increased, the homeostatic balance results in a pressure gradient difference at the lamina,” said Dunbar.

This seems to point to compromised autoregulation—that is, the body’s inability to regulate itself in the presence of changes that include vascular/postural changes, atmospheric pressure, temperature, fatigue, and resultant periods of ischemia that may occur and cause reduced or fluctuating IOP.

“Autoregulation or vascular dysregulation can lead to over- or underperfusion. Chronic underperfusion can lead to tissue necrosis or death, and unstable perfusion to oxidative stress,” he said.

These factors point to the possibility that something other than conventional IOP values may play a role in development of glaucoma.

The cumulative 20-year information gleaned from the all-important Ocular Hypertension Treatment Study indicated that approximately 30% of patients develop glaucoma over 20 years and various risk factors can increase that percentage significantly, such as older age, thinner cornea, and higher IOP.

In addition, conversion to POAG occurs unilaterally. Finally, most patients with ocular hypertension eventually require treatment.

“We recognize there are other factors besides IOP that infl uence the development/ progression of glaucoma. We are gaining more understanding of these other factors,” Dunbar said. However, for now, IOP is the factor that can be treated, he added.